Brower S T, Tartter P, Weiss S, Luderer A A, Lehrer S
Department of Surgery, Mount Sinai School of Medicine, New York, NY 10029, USA.
Mt Sinai J Med. 1995 Nov;62(6):419-21.
Breast cancer has a strong genetic component, and at least two breast cancer genes exist. But these genes probably play little role in most breast cancers. Other factors, such as environmental estrogens and diet, may cause the genetic changes involved in the genesis of sporadic breast cancer. A method of observing genetic changes indirectly might be to measure tumor markers known to be associated with breast cancer.
We measured, by biochemical extraction and partition, lipid-associated sialic acid in plasma (LASA-P), a circulating tumor marker, in a group of 239 women with benign or malignant breast tumors.
The concentration of LASA-P was elevated in women with both benign and malignant tumors and no family history of breast cancer (p = 0.046, one-way ANOVA). Because LASA-P levels rise with age and number of pregnancies, we analyzed our data using multiple linear regression. Benign versus malignant character of the tumor, family history of breast cancer, number of pregnancies, and age were the independent variables. Family history of breast cancer had a significant effect on LASA-P levels (p = 0.0146) independent of the effects of age (p = 0.011), number of pregnancies (0.012), and whether the tumor was benign or malignant (p = 0.31).
We hypothesize that elevated LASA-P in women with breast tumors and no family history of breast cancer is a result of the genetic changes occurring in nonfamilial breast cancer. These genetic changes, possibly related to environmental estrogens or other environmental factors, are distinct from the changes due to mutations of BRCA1 or other familial breast cancer genes. Moreover, the elevation of LASA-P suggests that the surface membranes of breast cancer may differ in composition. Further study may lead to exact characterization of the genetic and cell membrane changes associated with familial and nonfamilial breast tumors, and perhaps to better methods of breast cancer prevention and treatment.
乳腺癌具有很强的遗传因素，至少存在两种乳腺癌基因。但这些基因在大多数乳腺癌中可能作用不大。其他因素，如环境雌激素和饮食，可能导致散发性乳腺癌发生过程中涉及的基因变化。一种间接观察基因变化的方法可能是测量已知与乳腺癌相关的肿瘤标志物。
我们通过生化提取和分离，对一组239名患有良性或恶性乳腺肿瘤的女性测量了血浆中脂质相关唾液酸（LASA-P），一种循环肿瘤标志物。
在无乳腺癌家族史的良性和恶性肿瘤女性中，LASA-P浓度均升高（p = 0.046，单因素方差分析）。由于LASA-P水平随年龄和怀孕次数升高，我们使用多元线性回归分析数据。肿瘤的良性与恶性特征、乳腺癌家族史、怀孕次数和年龄为自变量。乳腺癌家族史对LASA-P水平有显著影响（p = 0.0146），独立于年龄（p = 0.011）、怀孕次数（0.012）以及肿瘤是良性还是恶性（p = 0.31）的影响。
我们推测，无乳腺癌家族史的乳腺肿瘤女性中LASA-P升高是散发性乳腺癌发生的基因变化所致。这些基因变化可能与环境雌激素或其他环境因素有关，不同于BRCA1或其他家族性乳腺癌基因突变引起的变化。此外，LASA-P升高表明乳腺癌的表面膜组成可能不同。进一步研究可能会准确描述与家族性和散发性乳腺肿瘤相关的基因和细胞膜变化，或许还能找到更好的乳腺癌预防和治疗方法。
